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dc.contributor.authorBorges, Mariana Eiras
dc.contributor.authorRibeiro, Alessandra Mussi
dc.contributor.authorPauli, José Rodrigo
dc.contributor.authorArantes, Luciana Mendonça
dc.contributor.authorLuciano, Eliete [UNESP]
dc.contributor.authorde Moura, Leandro Pereira
dc.contributor.authorde Almeida Leme, José Alexandre Curiacos
dc.contributor.authorMedeiros, Alessandra
dc.contributor.authorBertolini, Natália Oliveira [UNESP]
dc.contributor.authorSibuya, Clarice Yoshiko [UNESP]
dc.contributor.authorGomes, Ricardo José
dc.date.accessioned2018-12-11T17:30:55Z
dc.date.available2018-12-11T17:30:55Z
dc.date.issued2017-02-03
dc.identifierhttp://dx.doi.org/10.1016/j.neulet.2016.12.059
dc.identifier.citationNeuroscience Letters, v. 639, p. 157-161.
dc.identifier.issn1872-7972
dc.identifier.issn0304-3940
dc.identifier.urihttp://hdl.handle.net/11449/178560
dc.description.abstractThe Diabetes Mellitus (DM) is a chronic disease associated with loss of brain regions such as the cerebellum, increasing the risk of developing neurodegenerative diseases such as Parkinson's disease (PD). In the brain of diabetic and PD organisms the insulin/IGF-1 signaling is altered. Exercise training is an effective intervention for the prevention of neurodegerative diseases since it release neurotrophic factors and regulating insulin/IGF-1 signaling in the brain. This study aimed to evaluate the proteins involved in the insulin/IGF-1 pathway in the cerebellum of diabetic rats subjected to exercise training protocol. Wistar rats were distributed in four groups: sedentary control (SC), trained control (TC), sedentary diabetic (SD) and trained diabetic (TD). Diabetes was induced by Alloxan (ALX) (32 mg/kg b.w.). The training program consisted in swimming 5 days/week, 1 h/day, during 6 weeks, supporting an overload corresponding to 90% of the anaerobic threshold. At the end, cerebellum was extracted to determinate the protein expression of GSK-3β, IRβ and IGF-1R and the phosphorylation of β-amyloid, Tau, ERK1 + ERK2 by Western Blot analysis. All dependent variables were analyzed by one-way analysis of variance with significance level of 5%. Diabetes causes hyperglycemia in both diabetic groups; however, in TD, there was a reduction in hyperglycemia compared to SD. Diabetes increased Tau and β-amyloid phosphorylation in both SD and TD groups. Furthermore, aerobic exercise increased ERK1 + ERK2 expression in TC. The data showed that in cerebellum of diabetic rats induced by alloxan there are some proteins expression like Parkinson cerebellum increased, and the exercise training was not able to modulate the expression of these proteins.en
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.format.extent157-161
dc.language.isoeng
dc.relation.ispartofNeuroscience Letters
dc.sourceScopus
dc.subjectCerebellum
dc.subjectDiabetes
dc.subjectExercise
dc.titleCerebellar Insulin/IGF-1 signaling in diabetic rats: Effects of exercise trainingen
dc.typeArtigo
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.contributor.institutionCatholic University Center Unisalesiano
dc.contributor.institutionUniversity Center of Patos de Minas
dc.description.affiliationDepartment of Biosciences São Paulo Federal University (UNIFESP)
dc.description.affiliationSport Science Course University of Campinas UNICAMP
dc.description.affiliationDepartment of Physical Education São Paulo State University (UNESP)
dc.description.affiliationDepartment of Physical Education Catholic University Center Unisalesiano
dc.description.affiliationDepartament of Physical Education University Center of Patos de Minas
dc.description.affiliationUnespDepartment of Physical Education São Paulo State University (UNESP)
dc.identifier.doi10.1016/j.neulet.2016.12.059
dc.rights.accessRightsAcesso aberto
dc.description.sponsorshipIdCNPq: 142587/2007-9
dc.description.sponsorshipIdFAPESP: 2010/18257-0
dc.identifier.scopus2-s2.0-85008658889
dc.identifier.file2-s2.0-85008658889.pdf
dc.relation.ispartofsjr0,946
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